IL-10 Deficiency Accelerates Type 1 Diabetes Development via Modulation of Innate and Adaptive Immune Cells and Gut Microbiota in BDC2.5 NOD Mice.

ABSTRACT: Type 1 diabetes is an autoimmune disease caused by T cell-mediated destruction of insulin-producing β cells. BDC2.5 T cells in BDC2.5 CD4⁺ T cell receptor transgenic Non-Obese Diabetic (NOD) mice (BDC2.5 ⁺ NOD mice) can abruptly invade the pancreatic islets resulting in severe insulitis that progresses rapidly but rarely leads to spontaneous diabetes. This prevention of diabetes is mediated by T regulatory (Treg) cells in these mice. In this study, we investigated the role of interleukin 10 (IL-10) in the inhibition of diabetes in BDC2.5 ⁺ NOD mice by generating Il-10-deficient BDC2.5 ⁺ NOD mice (BDC2.5 ⁺ Il-10 ^-/- NOD mice). Our results showed that BDC2.5 ⁺

SUBMITTER: Huang J 

PROVIDER: S-EPMC8362616 | biostudies-literature | 2021

REPOSITORIES: biostudies-literature